Cancer metabolism articles within Nature

Featured

  • Letter |

    Mammalian mitochondria use folate-bound one-carbon units generated by the enzyme SHMT2 to methylate tRNA, and this modification is required for mitochondrial translation and thus oxidative phosphorylation.

    • Raphael J. Morscher
    • , Gregory S. Ducker
    •  & Joshua D. Rabinowitz

  • Letter |

    Mutations in the nucleotidase-encoding gene NT5C2 drive chemotherapy resistance in relapsed acute lymphoid leukaemia but the mutations also lead to a loss-of-fitness phenotype and to collateral drug sensitivity, which could be exploited for therapy.

    • Gannie Tzoneva
    • , Chelsea L. Dieck
    •  & Adolfo A. Ferrando

  • Article |

    LACTB modulates mitochondrial lipid metabolism and changes the differentiation state of breast cancer cells, thereby negatively affecting the growth of various tumorigenic, but not non-tumorigenic, cells both in vitro and in vivo.

    • Zuzana Keckesova
    • , Joana Liu Donaher
    •  & Robert A. Weinberg

  • Letter |

    The B-lymphoid transcription factors PAX5 and IKZF1 restrict the supply of glucose and energy to B cells to levels that are not enough to fuel a driver-oncogene, thereby acting as tumour suppressors and sensitizing acute lymphoblastic leukaemia B cells to glucocorticoid therapy.

    • Lai N. Chan
    • , Zhengshan Chen
    •  & Markus Müschen

  • Article |

    Human tumours with mutations in LKB1 and Kras have a specific hypermetabolic state associated with increased DNA methylation, pointing to potential metabolic and epigenetic vulnerabilities of specific tumours.

    • Filippos Kottakis
    • , Brandon N. Nicolay
    •  & Nabeel Bardeesy

  • Letter |

    Tumours can require certain amino acids for their proliferation, and the diricore method described here helps to identify such restrictive amino acids; using this method in kidney cancer tissue and breast carcinoma cells, the authors observe an association between proline deficiency and upregulation of PYCR1, an enzyme required for proline synthesis.

    • Fabricio Loayza-Puch
    • , Koos Rooijers
    •  & Reuven Agami

  • Letter |

    p53 is often mutated or lost in cancer; here inactivation of ΔNp63 and ΔNp73 in the absence of p53 is shown to result in metabolic reprogramming and tumour regression via activation of IAPP (islet amyloid polypeptide or amylin), and IAPP-based anti-diabetes therapeutic strategies show potential for the treatment of p53-deficient and mutant tumours.

    • Avinashnarayan Venkatanarayan
    • , Payal Raulji
    •  & Elsa R. Flores

  • Letter |

    KRAS mutations are a driver event of pancreatic ductal adenocarcinoma; here, a subpopulation of dormant tumour cells, relying on oxidative phosphorylation for survival, is shown to be responsible for tumour relapse after treatment targeting the KRAS pathway.

    • Andrea Viale
    • , Piergiorgio Pettazzoni
    •  & Giulio F. Draetta

  • Letter |

    Fructose-1,6-bisphosphatase is shown to be depleted in clear cell renal cell carcinoma (ccRCC) and inhibits ccRCC progression by antagonizing glycolytic flux in renal tubular epithelial cells and by restraining cell proliferation, glycolysis, and the pentose phosphate pathway in von Hippel–Lindau-protein-deficient ccRCC cells by blocking hypoxia-inducible factor function.

    • Bo Li
    • , Bo Qiu
    •  & M. Celeste Simon

  • Letter |

    Many patients with cancer experience cachexia, a wasting disorder of adipose tissue and skeletal muscle that leads to weight loss and frailty; now, tumour-derived parathyroid-hormone-related protein has been shown to stimulate the expression of genes involved in heat production in adipose tissues and to have an important role in tissue wasting.

    • Serkan Kir
    • , James P. White
    •  & Bruce M. Spiegelman

  • Letter |

    Gain-of-function mutations in isocitrate dehydrogenase (IDH) are among the most common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly cancer of the liver bile ducts; now mutant IDH is shown to block liver cell differentiation through the suppression of HNF-4α, a master regulator of hepatocyte identity and quiescence, leading to expansion of liver progenitor cells primed for progression to IHCC.

    • Supriya K. Saha
    • , Christine A. Parachoniak
    •  & Nabeel Bardeesy

  • Letter |

    A new mechanism by which acute myeloid leukaemia patients become resistant to Ara-C and a newer treatment, ribavirin, is uncovered; these drugs can be glucuronidated and thereby inactivated by members of the UDP glucuronosyltransferase family of enzymes activated through GLI1 signalling.

    • Hiba Ahmad Zahreddine
    • , Biljana Culjkovic-Kraljacic
    •  & Katherine L. B. Borden

  • Letter |

    New apparatus is used to maintain proliferating cancer cells in low-glucose conditions, demonstrating that mitochondrial oxidative phosphorylation (OXPHOS) is essential for optimal proliferation in these conditions; the most sensitive cell lines are defective in OXPHOS upregulation and may therefore be sensitive to current antidiabetic drugs that inhibit OXPHOS.

    • Kıvanç Birsoy
    • , Richard Possemato
    •  & David M. Sabatini

  • Letter |

    In mice with Eµ-myc transgenic lymphomas in which therapy-induced senescence (TIS) depends on the H3K9 histone methyltransferase Suv39h1, TIS-competent lymphomas but not TIS-incompetent Suv39h1– lymphomas show increased glucose utilization and ATP production after senescence-inducing chemotherapy to cope with proteotoxic stress elicited by factors of the senescence-associated secretory phenotype (SASP); senescent cancers are selectively vulnerable to drugs that block glucose utilization or autophagy.

    • Jan R. Dörr
    • , Yong Yu
    •  & Clemens A. Schmitt

  • Letter |

    Evidence for a link between cellular senescence and metabolic regulation is provided, through the observation that p53 represses the expression of malic enzymes, thereby regulating NADPH, lipid and glutamine metabolism; in turn, this repression further activates p53, promoting cellular senescence.

    • Peng Jiang
    • , Wenjing Du
    •  & Xiaolu Yang

  • News & Views |

    It is increasingly accepted that metabolic changes in cancer cells can drive tumour formation. The finding that the SIRT6 protein suppresses tumour formation by regulating metabolism adds weight to this view.

    • Luisa Tasselli
    •  & Katrin F. Chua

  • News & Views |

    A tightly regulated enzyme balances energy production and the synthesis of macromolecules from glucose in cancer cells. Upsetting this balance by stimulating the enzyme's activity can suppress tumour growth in mice.

    • Lei Jiang
    •  & Ralph J. DeBerardinis

  • News & Views |

    Cancer cells ignore oxygen availability, opting for less efficient, anaerobic ways of generating energy. The wisdom behind this choice seems to be in preventing the accumulation of reactive oxygen species, and so oxidative damage.

    • Nana-Maria Grüning
    •  & Markus Ralser

  • News and Views Q&A |

    Interest in the abnormal metabolism exhibited by cancer cells has been reawakened by the discovery of oncogenic mutations in metabolic enzymes, and by tools that monitor metabolism in living cells. Existing and emerging therapies aim to target this abnormal metabolism in various ways.

    • William G. Kaelin Jr
    •  & Craig B. Thompson

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